presentation on severe acute malnutrition

1. SEVERE ACUTE MALNUTRITION
DR. OBASOHAN EFE
DEPARTMENT OF PAEDIATRICS
GARKI HOSPITAL ABUJA
02/10/2019

2. OUTLINE
• Definitions
• Epidemiology
• Types of malnutrition
• Classification
• Causes of malnutrition
• Theories and pathophysiology of severe malnutrition
• Clinical presentation
• Investigations
• Treatment of severely malnourished patient / complications
• Differential diagnosis
• Prevention
• Prognosis and conclusion
• References

3. DEFINITION OF TERMINOLOGIES
• NUTRITION:
According to Black’s Medical Dictionary, nutrition is the process by which
the living organism physiologically absorbs and uses food to ensure
growth, energy production and repair of tissues.
• NUTRIENT:
According to Taber’s Cyclopedic Medical Dictionary, they are substance
that provides nourishment essential for the maintenance of life and
growth.

4. DEFINITION
• MALNUTRITION
 The WHO defines malnutrition as “the cellular imbalance between
the supply of nutrients and energy and the body’s demand for them
to ensure growth, maintenance and specific functions.”
 The term malnutrition encompasses both ends of the nutrition
spectrum, from undernutrition to overweight.

5. DEFINITION Contd.
• SEVERE ACUTE MALNUTRITION (SAM): is defined as
 severe wasting and/or bilateral edema.
 Severe wasting is extreme thinness diagnosed by a weight-for-length
(or height) below −3 SD of the WHO Child Growth Standards.
 In children ages 6-59 months, a mid-upper arm circumference <115
mm also denotes extreme thinness

6. ANTHROPOMETRY
• Nutritional status is often assessed in terms of anthropometry (measurement of
length/height, weight, mid upper arm circumference etc.)
• International standards of normal child growth under optimum conditions have
been established by the World Health Organization (WHO). These are available as
growth charts. There is also CDC growth chart
• The common measurements taken include: weight for age, weight for
length/height and mid upper arm circumference.
• Other measurements: skin fold thickness, waist hip ratio, Ponderal index, etc

7. GROWTH CHART
The WHO growth charts only provide information on
children up to 5 years of age
The CDC growth charts can be
used from ages 2-19 years

8. • HEIGHT FOR AGE (OR LENGTH FOR AGE IN CHILDREN < 2YEARS):
 This is a measure of linear growth
 Reduced height or length for age is called stunting.
 Stunting is impaired linear growth and It indicates chronic malnutrition
 The major risk period for growth stunting is between 4 and 24 months of age.
• WEIGHT FOR AGE AND WEIGHT FOR HEIGHT:
 This is the most commonly used index of nutritional status as it is easy to measure.
 Reduced weight for age or height is called wasting and is a measure of acute malnutrition
 Severe wasting (marasmus) is weight-for-height/length <-3 Z scores according to the 2006
WHO growth standards

9. • MID UPPER ARM CIRCUMFERENCE:
 The mid arm is midway of the distance
between the acromion process of the
scapula and the olecranon of the ulnar.
 It is measured in children from 6 months to 5 years.
 It is ideally measured using a Shakir strip which is
colour coded to make it easy.
 Interpretation: Normal/Green : >125mm
Borderline/yellow : 125mm-115mm
Severe/Red : <115mm

10. • BODY MASS INDEX:
 is calculated by dividing weight in kilograms by the square of height in meters.
 For children, BMI is age- and gender-specific. BMI-for-age can be used from birth to 20 years
 is a screening tool for thinness (<−2 SD), overweight (between +1 SD and +2 SD) and obesity
(>+2 SD).
Z-SCORE:
 This is a measure of how many standard deviations a data point is away from the mean
 Formula: Z = ( X – μ) / σ
Z = Z-score
X = figure / data point (E.g height for age)
μ = sample mean or median value (e.g median height)
σ = standard deviation (the square root of variance)
 The standards are applicable to all children everywhere

11. • FAILURE TO THRIVE:
 This is usually a diagnosis of children younger than 3 years of age,
 is considered if a child’s weight is below the 5th percentile, if it drops more than 2 major
percentile lines or if weight for height is less than the 5th percentile.
• PROTEIN-ENERGY MALNUTRITION (PEM)
 Refers to a range of pathological conditions arising from coincident lack of energy and/or
protein in varying proportions. (this terminology is no longer commonly used)
 It varies from mild through moderate to severe.
 The mild and moderate forms are mainly subclinical and are only detectable by
anthropometric methods of nutritional assessment and by biochemical test
 The severe forms include nutritional marasmus, kwashiorkor and marasmic kwarshiorkor

12. EPIDEMIOLOGY
• SAM affects nearly twenty million children under 5 years, causing up to 1 million deaths each
year by increasing susceptibility to death from severe infection
• Malnutrition underlies 54-55% of childhood mortality worldwide (10.8 million in Africa/year).
• The greatest risk of undernutrition occurs in the first 1000 days, from conception to 24 months
of age. (when growth velocity and brain development are especially high).
• The prevalence of Stunting is now highest in the African region (36% prevalence).
• Wasting (weight-for-height <−2 SD) affects 8% of children <5 years worldwide.
• Kwashiorkor: most commonly seen among children 1-3 years of age (when weaning off
breastmilk).
• Marasmus: more frequently seen in much younger children up to about the age of 3 ½ years.

13. EPIDEMIOLOGY contd.
Proportional mortality in children younger than five years old (source WHO 2004)

14. EPIDEMIOLOGY (NIGERIA)
 Nigeria’s Demographic and Health Survey (2013): Reports
I. An estimated 1.9 million children suffer from severe acute malnutrition
II. small improvements in rates of stunting: from 42 percent of children in 2003 to 37 percent of children in 2013
III. One out of every three Nigerian children is stunted (the second highest globally) and 7.8 percent of children are wasted
 The National Nutrition and Health Survey (NNHS) 2018:
I. the highest prevalence of acute malnutrition based on Mid Upper Arm circumference MUAC was reported in Zamfara
(10,3%) followed by Katsina with 8.5% while the lowest was recorded in Imo with 0.8%.
II. Kano State records the highest number of stunted children with 1.4 million in the North
 Prevalence of protein-energy malnutrition in Maiduguri , Nigeria ( Hamidu J.L et al. 2001). Results indicated:
I. the prevalence of marasmus was highest in the age group of 6 to 12 months in both sexes
II. Kwashiorkor was highest among the children in the 13 to 18 months age group in both males and females.
III. 80% of the mothers of the malnourished children had no formal education.

15. CLASSIFICATION OF UNDERNUTRITION
A. THE WELLCOME CLASSIFICATION:
• Uses weight for age index and
oedema for classication
• Good for clinical and acute
malnutrition
• Does not make use of height,
hence, it does not detect
stunting (chronic malnutrition)
• A child can be stunted but not
wasted

16. CLASSIFICATION OF UNDERNUTRITION
C. THE GOMEZ CLASSIFICATION:
• Also use weight for age index
• Does not make use of height,
hence, it does not detect
stunting (chronic malnutrition)
• Does not use oedema for
classification, hence a child
with oedema may be classified
as normal (increased weight)

17. CLASSIFICATION OF UNDERNUTRITION
C. THE WHO CLASSIFICATION: • Makes use of weight for height,
height for age and also considers
oedema.
• It can identify degree of acute
malnutrition (wasting) from weight
for height and chronic malnutrition
(stunting) from height for age.
• Also adopts standard deviation / Z-
score which have better statistical
precision in identifying deviation
from reference standards
• It’s the standard recommended for
global use for nutritional data

18. AETIOLOGY OF MALNUTRITION (UNDERNUTRITION)
• PEM is the outcome of the interaction of a number of complex and closely associated
factors that are related to:
1. The child
2. The socio-cultural economic circumstances of his family
3. The socio-political, technological and ecological structures of his community or country
• Theses diverse factors can be grouped under 3 levels of causality:
1. IMMEDIATE CAUSES: which directly affect the nutritional health status of the child
2. UNDERLYING CAUSES: that operate at the level of the family
3. REMOTE CAUSES: influencing the larger society

19. IMMEDIATE CAUSES (CHILD) UNDERLYING CAUSES (FAMILY) REMOTE CAUSES (COUNTRY)
a) Food intake
 Poor quality stable food:
Bulky, unpalatable, of low energy and
protein content e.g maize gruel
 Inadequate intake even when food is
available
b) Diseases / poor health
Interfere with food intake, digestion,
absorption, and utilization. E.g
 Measles
 Intestinal parasitosis
 HIV/AIDS
 Frequent respiratory tract infection
 Malaria etc
a) Insufficient household food security
1. Poverty
2. Unemployment (lack of income)
b) Inappropriate care for mothers:
1. Poor nutrition during pregnancy (lead to LBW
babies at risk of malnutrition)
2. Poor physical, mental and educational status
3. Lack of economic empowerment
4. Bad beliefs and superstition
5. Poor hygiene/weaning practice
6. Poor health seeking behavior
c) Inappropriate care for child:
1. Been born as LBW
2. One of a set of multiple birth
3. Lack of exclusive breastfeeding
4. Been cared for by other children
5. Congenital defects
6. Orphaned
d) Inadequate health care services and unhealthy
environment.
a) Political and ideological
structure
b) Cultural beliefs
c) Socio-economic
instability
d) Embezzlement of
allocations for health
care and the populace.

21. THEORIES / PATHOGENESIS OF SEVERE UNDERNUTRITION/PEM
• CLASSICAL THEORY (Dietetic hypothesis):
 Variable energy and protein deficiency
 This suggests that the cause of kwashiorkor is protein deficiency.
 This theory is supported by the work of Cicely Williams -introduced the name “Kwashiorkor”
in 1935 meaning “disease of the deposed child” in the Ga language of Gold Coast (Ghana).
 She observed that the babies were weaned onto starchy gruels, developed kwashiorkor and
were cured by milk.
• VITERI’S TIME BOUND THEORY:
 Long duration malnutrition leads to marasmus
 Abrupt and short duration of malnutrition leads to kwashiorkor

22. THEORIES / PATHOGENESIS OF SEVERE UNDERNUTRITION/PEM contd.
• FREE RADICAL THEORY:
 There is deficiency of anti-oxidant nutrients such as Vitamin A, C, E and selenium to neutralize
free oxygen radicals produced during various infections.
 In the presence of infection or aflatoxin, the accumulation of these toxic free radicals cause
damage to various organs including the liver.
• GOPALAN’S DYSADAPTATION THEORY:
 Biochemical adaptations leading to extreme catabolism and near normal anabolism results in
marasmus.
 Dysadaptations: failure of effective catabolism and failure of anabolism leads to kwashiorkor
• AFLATOXIN THEORY: aflatoxins which are toxic to the liver contaminates the diet.

23. THEORIES / PATHOGENESIS OF SEVERE UNDERNUTRITION/PEM contd.
• JELLIFFE’S HYPOTHESIS:
 A mixture of interactions and sequelae of dietary imbalances, infections and infestations,
emotional trauma and toxins
• ROLE OF INFECTION
 Kwarshiokor is often preceded by an episode of infection with diarrhoea and respiratory
infection. Others –measles, chicken pox, HIV, Whooping cough, TB, Malaria etc.
 Why does infection affect nutritional status?
– Poor appetite
– Dietary restriction –misconception of low feeds during diarrhoea.
– Malabsorption of nutrients
– Frank protein-losing enteropathy e.g. in measles, HIV.

24. THEORIES / PATHOGENESIS OF SEVERE UNDERNUTRITION/PEM contd.
• ROLE OF HORMONES:
 In kwashiorkor: Low plasma cortisol – Muscle protein NOT mobilized –Low plasma A.A –
stimulate the pituitary to secrete high GH – G.H is lypolytic causing high plasma free fatty acid
– low synthesis of lipoproteins – Fat accumulates in the liver – impaired hepatic fat
metabolism-Fatty liver.
 In marasmus: there is high plasma cortisol. Raised cortisol levels leads to breakdown of
muscle protein and the amino acids released are diverted to the liver for the synthesis of
plasma protein.
The plasma concentration of β-Lipoproteins is well maintained facilitating mobilization of
triglycerides from the liver .The metabolic integrity of the liver remains unimpaired in marasmus.

25. PATHOPHYSIOLOGY
• Children with severe acute malnutrition have had a diet insufficient in energy and nutrients
relative to their needs. The magnitude of the deficits will differ depending on:
 the duration of inadequacy,
 quantity and diversity of food consumed,
 presence of antinutrients (such as phytate),
 individual variation in requirements,
 and number and severity of coexisting infections and their duration.
• When a child’s intake is insufficient to meet daily needs, physiologic and metabolic changes
take place in an orderly progression to conserve energy and prolong life. This process is called
reductive adaptation.

26. PATHOPHYSIOLOGY
• REDUCTIVE ADAPTATION:
 Fat stores are mobilized to provide energy.
 Later protein in muscle, skin, and the gastrointestinal tract is mobilized.
 Energy is conserved by reducing physical activity and growth, reducing basal metabolism and
the functional reserve of organs and by reducing inflammatory and immune responses.
• CONSEQUENCES OF REDUCTIVE ADAPTATION / NUTRIENT DEFICIENCIES:
 The liver makes glucose less readily, making the child more prone to hypoglycemia
 The liver also produces less albumin, transferrin and other transport proteins.
 Heat production is less and coupled with loss of subcutaneous makes the child more

27. PATHOPHYSIOLOGY contd
• CONSEQUENCES OF REDUCTIVE ADAPTATION / NUTRIENT DEFICIENCIES contd:
 The kidneys are less able to excrete excess fluid and sodium, and fluid easily accumulates in
the circulation, increasing the risk of fluid overload.
 The heart is smaller and weaker and has a reduced output, and fluid overload readily leads to
death from cardiac failure.
 Sodium builds up inside cells due to leaky cell membranes and reduced activity of the
sodium/potassium pump, leading to excess body sodium, fluid retention, and edema.
 Potassium leaks out of cells and is excreted in urine, contributing to electrolyte imbalance,
fluid retention, edema, and anorexia.
 Loss of muscle protein is accompanied by loss of potassium, magnesium, zinc, and copper.

28. • CONSEQUENCES OF REDUCTIVE ADAPTATION / NUTRIENT DEFICIENCIES contd.
 The gut produces less gastric acid and enzymes. Motility is reduced and bacteria may colonize
the stomach and small intestines, damaging the mucosa and deconjugating bile acids.
Digestion and absorption are impaired.
 Cell replication and repair are reduced with the risk of bacterial translocation through the gut
 Immune function is impaired, especially cell mediated immunity. The usual response to
infection may be absent, even in severe illness (risk of undiagnosed infection)
 The red cell mass is reduced, releasing iron which requires glucose and amino acids to be
converted to ferritin, increasing the risk of hypoglycaemia and amino acid imbalances.
 Unbound iron promotes pathogen growth and formation of free radicals
 Micronutrient deficiencies limit the body’s ability to deactivates, which cause cell damage.
Oedema and hair/skin changes are outward signs of cell damage

29. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

30. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

31. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

32. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

33. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

34. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

35. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

36. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

37. • PATHOPHYSIOLOGY OF IMPORTANT CLINICAL FINDINGS:

38. CLINICAL PRESENTATION OF THE MALNOURISHED CHILD
• This depends on the severity or degree of undernutrition, aetiology and inter-current illness
• The child may have presented to the clinic for other complaints and discovered to be
malnourished on physical examination:
 prominent zygomatic bones and ribs, hanging skin folds like the baggy pant wasting around
the buttocks
 Oedematous: the oedema is peripheral and does not accumulate in serous cavities. Oedema
occurs in kwarshiokor and marasmic kwashiorkor unlike in marasmus alone
 Flaky paint dermatosis, protuberant abdomen, wizened facie, hair changes,
hepatosplenomegaly,
 They may present also with complications like hypothermia, hypoglycaemia, dehydration,
overwhelming sepsis,

39. CHECKLIST OF POINTS FOR TAKING THE CHILD’S MEDICAL HISTORY
• Usual diet before current episode of illness (24 hours diet recall and also the FADUS)
• AFASS (in the setting of breast milk substitute)
• Breastfeeding history
• Food and fluids taken in past few days
• Recent sinking of eyes
• Duration and frequency of vomiting or diarrhoea, appearance of vomit or diarrhoeal stools
• Time when urine was last passed
• Contact with people with measles or tuberculosis
• Any deaths of siblings
• Birth weight
• Milestones reached (sitting up, standing, etc.)
• Immunizations
• Level of education of the parents especially the mother
• Occupation of parents
• Communal food taboos / superstitions
• Any communal unrest e.g. from terrorism

40. HEAD TO TOE EXAMINATION OF THE SEVERELY MALNOURISHED CHILD
SITE SIGNS
HAIR Dull, sparse, brittle hair, hypopigmentation
Flag sign (alternating bands of light and normal color)
Broomstick eye lashes, alopecia
FACE Moon face (kwarshiorkor), simian facies (Marasmus)
Eye Dry eyes, pale conjunctiva,
Bitot spots, periorbital oedma
Mouth Angular stomatitis, cheilitis, glossitis,
spongy bleeding gums (vitamin C), parotid enlargement
Teeth Enamel mottling, delayed eruption
Skin Loose and wrinkled (marasmus), shiny and oedematous
(kwarshiorkor) , dry follicular hyperkeratosis, patchy hyper and
hypopigmentation (crazy paving or flaky paint dermatoses),
erosions, poor wound healing
Nails Koilonychia, thin and soft nail plates Fissures or ridges

41. HEAD TO TOE EXAMINATION OF THE SEVERELY MALNOURISHED CHILD contd
SITE SIGNS
Musculature Muscle wasting particularly buttocks and thighs
Chvostek or Trousseau sign (hypocalcemia)
Skeletal Deformities (usually from calcium, vitamin D or C deficiencies
Abdomen Distended: hepatomegaly with fatty liver;
ascites may be present
Cardiovascular Bradycardia, hypotension,
reduced cardiac output, small vessel vasculopathy
Neurologic Global developmental delay, loss of knee and ankle reflexes
Impaired memory
Haemotologic Pallor, petechiae, bleeding diathesis
Behavior Lethargic, apathetic,
Irritable on handling

45. INVESTIGATIONS
1. Specific investigations:
i. For suspected specific causes: e.g Genexpert for pulmonary TB, HIV screening, echocardiography for
congenital heart disease etc
2. Other investigations:
i. Random plasma glucose: for hypoglycaemia
ii. Full blood count: anemia, leukocytosis or leukopaenia, etc. In fact full sepsis screen.
iii. Serum albumin, total protein, serum calcium and phosphate.
iv. Electrolyte, urea and creatinine: dyselectrolytaemia like hypokalemia
v. Serum ferritin and red cell indices
vi. Urine and stool mcs
vii. Imaging:Abdominal ultrasound: hepatomegaly; Chest x-ray: consolidations, fractures, etc.

46. TREATMENT
• This is multidisciplinary: paediatricians, dietiticians, social welfare, etc.
• Those without complications can have outpatient care:
i. Oedema is +/++
ii. MUAC > 115 mm
iii. Good appetite (indicates less metabolic disturbance), clinically well and alert
• Indications for inpatient care (those with complications):
i. Severe oedema (+++)
ii. MUAC <115mm
iii. Those with anorexia, clinically unwell and not alert

47. TREATMENT contd.
1. Resuscitation / emergency treatment / stabilization:
i. Prevent / treat hypoglycaemia
ii. Prevent / treat hypothermia
iii. Prevent /treat dehydration / correct imbalance of electrolyte especially severe
hypokalemia
iv. Start the treatment of infections
2. Rehabilitation
3. Follow up

48. TEN STEPS OF TREATMENT FOR SEVERE ACUTE MALNUTRITION

49. STEPS OF TREATMENT FOR SEVERE ACUTE MALNUTRITION
Source: WHO Management of Severe Malnutrition: a manual for physicians and other senior health workers

50. PREVENTION AND TREATMENT OF HYPOGLYCAEMIA IN SEVERE ACUTE MALNUTRITION
 IF THERE IS HYPOGLYCAEMIA (BLOOD GLUCOSE <3MMOL/L) AND THE CHILD IS UNCONSCIOUS:
 Immediately give sterile 10% glucose (5 mL/kg) by intravenous route
 Feed every 2 hours for at least first day. Initially give 1/4 of feed every 30 min. Use NG-tube if unable to drink
 Keep warm and commence broad spectrum antibiotics
 WHEN THERE IS HYPOGLYCAEMIA AND THE CHILD IS CONSCIOUS:
 10% glucose, or start feeds, or 1 teaspoon sugar under the tongue-whichever is quickest
 Feed every 2 hours for at least the first day. Initially give 1/4 of feed every 30 min
 HOW TO PREVENT HYPOGLYCAEMIA:
 Avoid long gaps without food. Feed every 3 hours day and night (2 hourly if ill)
 Feed on time and keep warm. Treat infections as hypoglycaemia and hypothermia may be signs of infection

51. PREVENTION AND TREATMENT OF HYPOTHERMIA
 HYPOTHERMIA IS AXILLARY <35°C (95°F); RECTAL <35.5°C (95.9°F) : they die at night (temperature at nadir)
 TREATMENT OF HYPOTHERMIA ( ACTIVE REWARMING IS NEEDED)
 Skin-to-skin contact with carer (“kangaroo technique”)
 dress in warmed clothes, cover head, wrap in warmed blanket
 Provide indirect heat (e.g. heater; transwarmer mattress; incandescent lamp)
 Monitor temperature hourly (or every 30 min if using heater) and stop rewarming when rectal temperature is
36.5°C (97.7°F)
 PREVENTION OF HYPOTHERMIA:
 Avoidance of exposure: Dress warmly, including head and cover with blanket
 Change wet clothes and bedding
 Keep room hot. Treat infections, feed frequently and do not bath if ill.

52. PREVENTION AND TREATMENT OF SHOCK
 IF IN SHOCK (THIS MAY BE FROM HYPOVOLEMIA OR SEPTIC SHOCK):
 that treatment of shock in these children is different (less rapid, smaller volume, different fluid) from treatment
of shock in well-nourished children.
 shock from sepsis and dehydration often co-exists. One has to be guided by the response to treatment.
 children with shock from dehydration respond to IV fluid whereas those with septic shock will not respond.
 Since severely malnourished children can quickly succumb to fluid overload, they must be monitored closely.
 SIGNS OF SHOCK:
i. Lethargic or unconscious
ii. Cold extremities. Peripheral and core temperature dissociation
iii. Capillary refill > 3 seconds
iv. Weak, fast pulse. Note: hypotension is a late sign.

53.  TREATMENT OF SHOCK IN SEVERE ACUTE MALNUTRITION:
 Give oxygen
 Give sterile 10% glucose (5 mL/kg) intravenously
 Give IV fluid at 15 mL/kg over 1 hour, using Ringers lactate with 5% dextrose or half-normal saline with 5%
dextrose or half-strength Darrow solution with 5% dextrose. If these are unavailable use Ringer’s lactate.
i. IF THERE IS NO IMPROVEMENT ASSUME SEPTIC SHOCK, THEN
- Commence maintenance IV fluid at 4ml/kg/hour while waiting for blood
- 10 mL/kg fresh whole blood and transfuse slowly over 3 hr. If signs of heart failure, give 5-7 mL/kg packed cells
rather than whole blood. Give frusemide at the start of transfusion.
ii. IF THERE ARE SIGNS OF IMPROVEMENT (PULSE AND RESPIRATION RATES FALL):
- Repeat IVF 15 mL/kg for 1 more hour. Then switch to oral or nasogastric rehydration with ReSoMal, 5-10 mL/kg
in alternate hour

54. PREVENTION AND TREATMENT OF SEVERE DEHYDRATION contd.
 DO NOT GIVE IV FLUIDS EXCEPT THE CHILD IS IN SHOCK
 Give ReSoMal 5 mL/kg every 30 minutes for first 2 hours orally or via NG tube
 Then give 5-10 mL/kg in alternate hours for up to 10 hr. Amount depends on stool loss and eagerness to drink.
Feed in the other alternate hour
 Monitor hourly and stop if signs of overload develop:
i. pulse rate increases by 25 beats/min and respiratory rate by 5 breaths/min;
ii. increasing edema; engorged jugular veins
 Stop when rehydrated: when there are 3 or more signs of hydration:
i. less thirsty, passing urine, skin pinch less slow,
ii. eyes less sunken, moist mouth, tears, less lethargic, improved pulse and respiratory rate).
 PREVENTION OF DEHYDRATION: replace ongoing loss e.g. from loose stool

55. If Resomal is not immediately available, it can be prepared by adding the WHO
standard ORS to 2L of water, then add potassium chloride (20mmol/L + 20mmol
in standard ORS to make it 40mmol and 50 grams of sucrose (one heap teaspoon
of granulated sugar). Add mineral solution if available

56. BLOOD TRANSFUSION IN SEVERE ACUTE MALNUTRITION
 INDICATIONS FOR BLOOD TRANSFUSION:
i. In very severe anaemia (Haemoglobin < 4 g/dL)
ii. If anemic and haemoglobin is between 4 – 6 g/dL with respiratory distress
iii. Failure to respond to fluid resuscitation in septic shock.
 HOW TO TRANSFUSE THESE CHILDREN:
 Give whole blood 10 mL/kg slowly over 3 hours.
 If there are signs of heart failure, give 5-7 mL/kg packed cells rather than whole blood
 Give furosemide 1 mL/kg IV at the start of the transfusion

57. MANAGEMENT OF DYSELECTROLYTAEMIA AND MICRONUTRIENT DEFICIENCIES IN SEVERE ACUTE MALNUTRITION
 THERE IS DEFICIT OF POTASSIUM AND MAGNESIUM BUT EXCESS SODIUM:
 Give extra potassium (4 mmol/kg/day) for at least two weeks
 Magnesium (0.4 to 0.6 mmol/kg/day) for at least 2 weeks
 MICRONUTRIENTS:
 Give vitamin A on day 1 (under 6 mo 50,000 units; 6-12 mo 100,000 units; >12 mo 200,000 units) if child has any
eye signs of vitamin A deficiency or has had recent measles. Repeat this dose on days 2 and 14
 Folic acid 1 mg daily but give 5 mg on day 1.
 Zinc (2 mg/kg/day)
 Combined Mineral Vitamin mix (CMV) and can be added to feeds and ReSoMal
 Multivitamin syrup.
 IRON SUPPLEMENTATION (3mg/kg/day) IS DELAYED UNTIL WEIGHT GAIN BECOMES EVIDENT AND ALL
ASSOCIATED INFECTIONS BROUGHT UNDER CONTROL; usually started from the second week of treatment.

58. TREATMENT OF INFECTIONS IN SEVERE ACUTE MALNUTRITION
 INFECTIONS ARE OFTEN SILENT. Starting on the first day, give broadspectrum antibiotics to all children.
1. If there are no complications:
- Amoxicillin oral 25 mg/kg/dose twice daily for 5 days
2. If there are complications: (shock, hypoglycemia, hypothermia, skin lesions, respiratory or urinary tract
infections, or lethargy/sickly)
Gentamicin (7.5 mg/kg IV or IM) once daily for 7 days
and
Ampicillin (50 mg/kg IV or IM) every 6 hours for 2 days, then oral amoxicillin (25-40 mg/kg/dose) every 8 hoursr
for 5 days
 IF SPECIFIC INFECTIONS ARE IDENTIFIED, ADD APPROPRIATE ANTIBIOTICS. Cover for Gram negative organisms
 FOR PERSISTENT DIARRHEA/SMALL BOWEL OVERGROWTH, add metronidazole (7.5 mg/kg oral) every 8 hours
for 7 days.
 Deworm (eliminate intestinal parasitic infections): Give oral mebendazole 100mg daily for 3 days

59. PREVENTION OF INFECTIONS IN SEVERE ACUTE MALNUTRITION
 MINIMIZE RISK OF CROSS-INFECTION:
Avoid overcrowding
Wash hands
 COVER SKIN LESIONS SO THEY DO NOT BECOME INFECTED: barrier cream such as zinc oxide
and castor oil
 TOPICAL CARE OF SORES using 0.01% potassium permanganate solution
 KEEP THE SKIN DRY.
 GIVE MEASLES VACCINE TO UNIMMUNIZED CHILDREN > 6 months of age.

60. FEEDING IN SEVERE ACUTE MALNUTRITION
 The altered metabolic status of the severely malnourished child makes him much less capable
of tolerating the usual amounts of fat, protein and sodium in normal formula (milk) diet.
 Deterioration of the child’s condition can be realized if re-feeding is started with formula diets
that are low in these nutrients but are high in energy (carbohydrate) content and density
 The formula diets are essentially based on dried skimmed milk (low fat).
Generally they are referred to as high energy milk or mixture
 F-75 (starter feed): used during the initial phase of treatment
F-100: for catch up growth.
Feeding is started cautiously. There is gradual increment with the child encouraged to eat as
often as possible until the ultimate intake of 150-220 kcal/kg/day. If taking ≤80% of feeds
offered, feed via NG-tube.

61. FEEDING IN SEVERE ACUTE MALNUTRITION
 In the initial phase:
 Give 8-12 small feeds of F75 to provide 130ml/kg/day, 100kcal/kg/day &1-1.5g protein/kg/day
 If gross edema, reduce volume to 100 ml/kg/day.
 Keep a 24-hr intake chart: measure feeds carefully and record leftovers.
 Encourage continued breastfeeding.
 Transfer to F100 when appetite returns (usually within 1 week) and edema has been lost or is
reduced (the nutritional rehabilitation phase). Transition is made slowly
 The milk based diet is gradually replaced with locally available foods which are fortified with
food items drawn from the different food groups (dietary diversification)
 Weigh daily and plot weight.

63. REFEEDING SYNDROME COMPLICATING FEEDING IN SEVERE ACUTE MALNUTRITION
 When excessive carbohydrates are administered, the resultant increase in serum insulin levels
may produce hypokalemia, hypophosphatemia, and hypomagnesemia
 The hallmark of refeeding syndrome is the development of severe hypophosphatemia after
the cellular uptake of phosphate during the first week of starting to refeed.
 Serum phosphate levels of ≤0.5 mmol/L can produce weakness, rhabdomyolysis, neutrophil
dysfunction, cardiorespiratory failure, arrhythmias, seizures, altered level of consciousness, or
sudden death.
 PREVENTION:
i. Follow WHO recommendations for treatment malnutrition.
ii. Avoid aggressive enteral or parenteral alimentation
iii. Monitor serum phosphate levels during refeeding.

64. SENSORY STIMULATION AND EMOTIONAL SUPPORT
 This is particularly necessary when delayed mental and behavioral development is present.
 It is necessary to provide:
i. Tender loving care (TLC)
ii. Cheerful, stimulating environment
iii. Structured play therapy 15-30 minutes per day
iv. Physical activity as soon as the child is well enough. Provide suitable toys.
v. Maternal involvement when feasible: e.g. comforting, feeding, bathing, skin to skin care, eye
to eye contact, etc.

65. MONITORING OF PATIENT DURING TREATMENT OF SEVERE MALNUTRITION: WHAT TO EXPECT
 Good weight gain: >10 g/kg/day
 Moderate weight gain: 5-10 g/kg/day. Check intake and infection
 Poor weight gain: (< 5 g/kg/day): causes include
i. Inadequate feeding
ii. Untreated infection
iii. Specific nutrient deficiencies: e.g dermatitis, diarrhea, dementia and death from pellagra
iv. Psychological problems
v. Poorly equipped health care facilities with ill-motivated staff.

66. MONITORING OF PATIENT DURING TREATMENT OF SEVERE MALNUTRITION: WHAT TO EXPECT
Signs of response to treatment include:
i. Eating well
ii. Mental state has improved: smiles, responds to stimuli, interested in
surroundings
iii. Sits, crawls, stands or walks (depending on age)
iv. Normal temperature (36.5–37.5 °C)
v. No vomiting or diarrhoea
vi. No oedema
vii.Gaining weight: >5 g/kg of body weight per day for 3 successive days

67. CRITERIA TO DISCHARGE THE PATIENT WITH SEVERE ACUTE MALNUTRITION
1. Recovered: Attain ≥ 90% weight for length / ≥ -1 SD and no oedema
2. Absence of infection
3. Eating at least 120-130 kcal/kg/day and receiving adequate micronutrients
4. Consistent weight gain (at least 5 g/kg/day for 3 consecutive days on exclusive oral feeding
5. Complete immunization appropriate for age
6. Caretakers sensitized to home care.

68. FOLLOW UP AFTER DISCHARGE
 Planned follow-up of the child at regular intervals after discharge is essential
 As the risk of relapse is greatest soon after discharge, the child should be seen after 1 week, 2
weeks, 1 month, 3 months and 6 months. After 6 months, visits should be twice yearly until
the child is at least 3 years old.
 Provided the child’s weight-for-height is not less than -1SD (90%) of the median NCHS/WHO
reference values, progress is considered satisfactory.
 At each visit:
I. the mother should be asked about the child’s recent health, feeding practices, play activities
II. The child should be examined, weighed and measured, and the results recorded
III. Any needed vaccine should be given
IV. Training of the mother should focus on areas that need to be strengthened e.g feeding
practices, and mental and physical stimulation of the child.
V. Attention should also be given to feeding practices for other children in the family

69. MONITORING OF PATIENT DURING TREATMENT OF SEVERE MALNUTRITION: contd
 Primary failure to respond to treatment:
i. Failure to regain appetite by day 4
ii. Failure to start losing oedema by day 4
iii. Presence of oedema on day 10
iv. Failure to gain at least 5 g/kg/day by day 10.
 Secondary failure to respond:
Failure to gain at least 5 g/kg/day for 3 consecutive days during rehabilitation.

70. DIFFERENTIAL DIAGNOSIS
1. Nephrotic syndrome: tetrad of massive proteinuria, hypoalbuminemia, generalized oedema and hyperlipidemia
2. Heart failure especially from congenital heart disease: tachyppnoea, tachycardia, tender hepatomegaly, gallop
rhythm, easy fatigability, etc
3. Chronic liver disease: nodular liver, gynecomastia, spider nevi, palmar erythema, ascites, etc
4. Chronic renal failure: nocturia, polyuria, GFR < 30ml/min/1.73m2, elevated urea/creatinine, hyperkalemia, etc
5. Chronic pancreatitis
6. Tumour induced cachexia
7. Hyperthyroidism: exophthalmos, goiter, sweaty, lid lag, weight loss in spite of voracious appetite, etc
8. Muscular dystrophies: example is spinal muscular atrophy (Werdnig-Hoffmann disease, Kugelberg Welander
disease) where there is severe hypotonia, wasting of proximal muscles but the extra-ocular muscles are spared).
They are alert, bright but weak. They can be confused for nutritional marasmus.
9. Inborne errors of amino acid and lipid metabolism.

71. PREVENTION OF SEVERE ACUTE MALNUTRITION
 GENERAL HEALTH PROMOTION: growth monitoring to identify faltering, eat variety of foods
 SPECIFIC PROPHYLAXIS:
 immunization against diseases like measles, tuberculosis.
 Breast feeding, good maternal nutrition during gestation to prevent low birth weight
 EARLY DIAGNOSIS AND TREATMENT: appropriate antibiotics; food fortification, deworm, etc
 LIMITATION OF DISABILITY: vitamin A and atropine drops for corneal ulcer; zinc oxide cream
for wounds, micronutrients supplementation
 REHABILITATION :
 Gradual feeding, provide stimulating environment, monitor response to treatment, etc

72. PREVENTION OF SEVERE ACUTE MALNUTRITION contd.
These and other preventive steps can be summarized by the child survival strategies:
GOBI FFF EETH (by UNICEF /world bank)
 Growth monitoring
 Oral rehydration therapy
 Breastfeeding
 Immunisations
 Family planning
 Female education
 Food fortification
 Environmental sanitation
 Essential drugs
 Treatment of common childhood diseases
 Health education

73. PROGNOSIS AND CONCLUSION
POOR PROGNOSTIC CRITERIA IN PROTEIN ENERGY MALNUTRITION
1. Age: infants 8. Signs of CCF / Respiratory distress
2. Weight for height <70% /-3SD 9. Total serum protein < 3 g/dL & albumin < 2 g/dL
3. MUAC <11.5cm 10. Severe anaemia with clinical signs of hypoxia
4. Stupor or coma 11. Extensive exudative or exfoliative dermatosis
5. Severe Gram negative sepsis 12. Hypoglycaemia
6. Haemorrhagic tendencies 13. Hypothermia
7. Thrombocytopaenia 14. Low gamma globulin fraction

74. PROGNOSIS AND CONCLUSION contd.
 The outcome is influenced by the underlying cause and the severity.
 Typically, children treated in the community with uncomplicated SAM have a case fatality of
less than 5%.
 Children treated as inpatients (complicated SAM) – usually because of severe infections
including pneumonia, diarrhoea, sepsis or HIV, have a reported case fatality of 10 to 40%.
 Most mortality amongst hospitalized cases tend to occur within the first 3 days of admission
 Successful management requires frequent, careful clinical evaluation and anticipation of
common problems so they can be prevented, or recognized and treated at an early stage.

75. REFERENCES
1. Nelson Textbook of paediatrics 20th edition
2. Paediatrics and child health in a tropical region 2nd edition Azubuike and Nkanginieme
3. Protein energy malnutrition & severe acute malnutrition. IAP UG Teaching slides 2015-2016
4. PEDIBLOOM: paediatric cases and summaries
5. https://www.who.int/selection_medicines/committees/expert/21/applications/s6_paed_antibiotics_appendix7_sam.pdf
6. Black RE, Victora CG, Walker SP, et al. Maternal and child undernutrition and overweight in low-income and middle-income
countries. Lancet. 2013;382(9890):427-451.
7. World Health Organization. Updates on the management of severe acute malnutrition in infants and children. WHO;2013.
9789241506328.
8. World Health Organisation. Management of Severe Malnutrition: a manual for physicians and other senior health workers.
Geneva: World Health Organisation;1999.
9. https://www.who.int/quantifying_ehimpacts/publications/MalnutritionEBD12.pdf
10. https://apps.who.int/iris/bitstream/handle/10665/41999/a57361.pdf;jsessionid=53BBE8ED9A64C33346567F278A552493?se
quence=1
11. https://wicworks.fns.usda.gov/resources/wic-growth-charts
12. https://www.cdc.gov/growthcharts/who_charts.htm
13. https://www.unicef.org/nigeria/nutrition
14. https://www.spring-nutrition.org/publications/reports/assessing-drivers-malnutrition-nigeria
15. severeacutemalnutritionbymoracha-141021092622-conversion-gate02